Mind the Gap in Acute Pancreatitis: Alcoholic, Triglycerides, or Kabadi?
Poster #: 051
Session/Time: B
Author:
Zi Guo, MS
Mentor:
Matt Slief, MD
Research Type: Case Report
Abstract
INTRODUCTION:
Ketoacidosis is characterized by the accumulation of ketone bodies resulting in metabolic acidosis. While diabetic ketoacidosis is the most frequent form, in the case of pancreatitis, non-diabetic causes such as alcoholic ketoacidosis, starvation ketoacidosis in the setting of hypertriglyceridemia, and the less-recognized Kabadi syndrome must also be considered. Distinguishing between these entities is essential, as their underlying mechanisms and etiologies differ.
CASE INFORMATION:
A 31-year-old male with a history of heavy alcohol use presented with severe, progressive midepigastric pain radiating to the back with associated reduced oral intake, beginning two days after his last alcohol drink. He reported binge drinking ~12 standard drinks several times per week and denied chronic medical conditions. Initial labs: WBC 15.3 ×10⁹/L, lipase 673 U/L, ALP 124 U/L, bilirubin 1.3 mg/dL. CT abdomen/pelvis revealed peritoneal fluid around the pancreas, duodenum, and right paracolic gutter. He received 2L Lactated Ringer's and was admitted for acute pancreatitis, meeting 3/3 diagnostic criteria. Further labs included triglycerides 2401 mg/dL and ethanol level <0.01 g/dL. Although the patient's initial anion gap was normal, ketoacidosis was identified 8 hours later with an anion gap of 22 (HCO₃⁻ 12) and β-hydroxybutyrate 7.5 mg/dL. Triglycerides spontaneously declined from 2401 mg/dL to 1275 mg/dL, coinciding with the development of the anion gap. Plasmapheresis, insulin, and dextrose were later initiated, resulting in further reduction of triglycerides to 382 mg/dL, resolution of the anion gap, and significant clinical improvement.
DISCUSSION/CLINICAL FINDINGS:
Physiologic principles were reviewed in efforts to diagnose the source of the patient's ketoacidosis. Alcoholic ketoacidosis typically occurs in chronic alcohol users after binge drinking followed by fasting. This results in glycogen depletion and an increased NADH/NAD⁺ ratio with impaired gluconeogenesis, leading to ketone accumulation. Hypertriglyceridemia in the setting of starvation may also contribute to ketoacidosis as abundant triglycerides are broken down into free fatty acids and metabolized to ketoacids in the liver. Kabadi syndrome is a rare form of ketoacidosis associated with severe acute pancreatitis. It has been proposed that Kabadi syndrome is driven primarily by pancreatic lipase-mediated accelerated lipolysis, correlating with pancreatitis severity. In this case, the diagnostic challenge centered on the source of the transient anion gap. While historical features including binge drinking, fasting, and profound hypertriglyceridemia support alcoholic and starvation mechanisms, the severity of the pancreatitis and lipase elevation could support Kabadi syndrome as well. Ultimately, it is not feasible to definitively determine whether the sharp triglyceride decline (2401 → 1275 mg/dL) and subsequent anion gap was mediated by lipase-driven lipolysis or hormonal effects. Base rate supports alcoholic and starvation contributions; however each process may have contributed and the mechanisms driving pancreatic ketoacidosis remain incompletely understood.
CONCLUSION:
This case highlights the diagnostic challenge of differentiating Kabadi syndrome from alcoholic and starvation ketoacidosis in patients with alcohol use and acute pancreatitis, particularly when the source of the transient anion gap is unclear. All three mechanisms-alcohol-induced shifts in glucose metabolism, hypertriglyceridemia with conversion to ketoacids, and pancreatitis-driven lipolysis as described in Kabadi syndrome-can result in increased ketone production leading to ketoacidosis.
Ketoacidosis is characterized by the accumulation of ketone bodies resulting in metabolic acidosis. While diabetic ketoacidosis is the most frequent form, in the case of pancreatitis, non-diabetic causes such as alcoholic ketoacidosis, starvation ketoacidosis in the setting of hypertriglyceridemia, and the less-recognized Kabadi syndrome must also be considered. Distinguishing between these entities is essential, as their underlying mechanisms and etiologies differ.
CASE INFORMATION:
A 31-year-old male with a history of heavy alcohol use presented with severe, progressive midepigastric pain radiating to the back with associated reduced oral intake, beginning two days after his last alcohol drink. He reported binge drinking ~12 standard drinks several times per week and denied chronic medical conditions. Initial labs: WBC 15.3 ×10⁹/L, lipase 673 U/L, ALP 124 U/L, bilirubin 1.3 mg/dL. CT abdomen/pelvis revealed peritoneal fluid around the pancreas, duodenum, and right paracolic gutter. He received 2L Lactated Ringer's and was admitted for acute pancreatitis, meeting 3/3 diagnostic criteria. Further labs included triglycerides 2401 mg/dL and ethanol level <0.01 g/dL. Although the patient's initial anion gap was normal, ketoacidosis was identified 8 hours later with an anion gap of 22 (HCO₃⁻ 12) and β-hydroxybutyrate 7.5 mg/dL. Triglycerides spontaneously declined from 2401 mg/dL to 1275 mg/dL, coinciding with the development of the anion gap. Plasmapheresis, insulin, and dextrose were later initiated, resulting in further reduction of triglycerides to 382 mg/dL, resolution of the anion gap, and significant clinical improvement.
DISCUSSION/CLINICAL FINDINGS:
Physiologic principles were reviewed in efforts to diagnose the source of the patient's ketoacidosis. Alcoholic ketoacidosis typically occurs in chronic alcohol users after binge drinking followed by fasting. This results in glycogen depletion and an increased NADH/NAD⁺ ratio with impaired gluconeogenesis, leading to ketone accumulation. Hypertriglyceridemia in the setting of starvation may also contribute to ketoacidosis as abundant triglycerides are broken down into free fatty acids and metabolized to ketoacids in the liver. Kabadi syndrome is a rare form of ketoacidosis associated with severe acute pancreatitis. It has been proposed that Kabadi syndrome is driven primarily by pancreatic lipase-mediated accelerated lipolysis, correlating with pancreatitis severity. In this case, the diagnostic challenge centered on the source of the transient anion gap. While historical features including binge drinking, fasting, and profound hypertriglyceridemia support alcoholic and starvation mechanisms, the severity of the pancreatitis and lipase elevation could support Kabadi syndrome as well. Ultimately, it is not feasible to definitively determine whether the sharp triglyceride decline (2401 → 1275 mg/dL) and subsequent anion gap was mediated by lipase-driven lipolysis or hormonal effects. Base rate supports alcoholic and starvation contributions; however each process may have contributed and the mechanisms driving pancreatic ketoacidosis remain incompletely understood.
CONCLUSION:
This case highlights the diagnostic challenge of differentiating Kabadi syndrome from alcoholic and starvation ketoacidosis in patients with alcohol use and acute pancreatitis, particularly when the source of the transient anion gap is unclear. All three mechanisms-alcohol-induced shifts in glucose metabolism, hypertriglyceridemia with conversion to ketoacids, and pancreatitis-driven lipolysis as described in Kabadi syndrome-can result in increased ketone production leading to ketoacidosis.